Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies
نویسندگان
چکیده
منابع مشابه
β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure
Although β-adrenoceptor (β-AR) blockade is an important mode of therapy for congestive heart failure (CHF), subcellular mechanisms associated with its beneficial effects are not clear. Three weeks after inducing myocardial infarction (MI), rats were treated daily with or without 20 and 75 mg/kg atenolol, a selective β(1) -AR antagonist, or propranolol, a non-selective β-AR antagonist, for 5 wee...
متن کاملCardiac Hypertrophy and Heart Failure
In cardiac and skeletal muscle, the sarcoplasmic reticulum (SR) plays a central role in the contraction relaxation cycle of the muscle by virtue of its ability to regulate the intracellular free Ca'+ concentration [Ca'+],. Ca'+ release from the SR increases [Ca'+] (10`mol/L), thus inducing contraction, whereas Ca2` uptake by the SR reduces [Ca'+] (=10-7 mol/L), producing muscle relaxation. In c...
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Primary heart failure in cardiomyopathy occurs in (1) hypertrophic cardiomyopathy, a genetic disease of the sarcomere; and (2) in dilated cardiomyopathy. The latter is often regarded as idiopathic in origin, but requires exclusion of all possible etiologies which are becoming easier to identify with modern investigative techniques. Tachycardia-induced cardiomyopathy is now increasingly recogniz...
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AIMS Cardiac hypertrophy and heart failure are associated with QT prolongation and lethal ventricular arrhythmias resulting from decreased K(+) current densities and impaired repolarization. Recent studies in mouse models of physiological cardiac hypertrophy revealed that increased phosphoinositide-3-kinase-α (PI3Kα) signalling results in the up-regulation of K(+) channels and the normalization...
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Cardiac remodelling occurs in response to stress, such as chronic hypertension or myocardial infarction, and forms the substrate for subsequent development of heart failure. Key pathophysiological features include ventricular hypertrophy, interstitial fibrosis, contractile dysfunction, and chamber dilatation. Although the molecular mechanisms are complex and not fully defined, substantial evide...
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ژورنال
عنوان ژورنال: Canadian Journal of Cardiology
سال: 2006
ISSN: 0828-282X
DOI: 10.1016/s0828-282x(06)70315-4